ProgrramDirierecctotor/rP/PrinricnicpiapllanlvIensvteigsattigorat(oLras(Lt,aFsirts,tF, iMrsidt,dMle)id: dCleh):ieCnh,ienY,uYeuheh-H-Hsiu 1I R0O1l A1I080829-0O1A1I thqtthese cells act early in host immune defense. explored. We will been well documented, little is known about how IL-17 is regulated although deficier)tol;JT responses have been noted in 17+ population at the onset of CFA immunization. While the development of IL-17:tDI;JT cells has Our previous experiments suggested that 0 I;JT cells are uniquely suited to mount an investigate these areas, which an inflammatory response to affect the priming process has not been .L., are of fundamental importance in mice lackingDI;JT cells, the possibility in DI;:JT cells. cells are the major IL- Furthermore, understanding ABSTRACT Inflammation is a rapid response to tissue damage and/or infection. While it is largely an innate response during its initial stages, in vertebrates, it has evolved to require a T ceU cytokine, IL-17, to promote the expansion of neutrophils and monocytes in the bone marrow and their release and recruitment to sites of inflammation. This process strengthens the inflammatory cascade to eradicate the injurious signal, starts the resolution program and launches the adaptive immune response. Our previous experiments suggested that El EIIT cells are uniquely suited to mount an IL-17 response at the onset of acute inflammation and we found that E1II1J cells are the major IL- 17+ population at the onset of CFA immunization. While the development of IL-i 7f Li LIT cells has been well documented, little is known about how IL-17 is regulated in[ILIT cells. Furthermore, although deficientLi LiT responses have been noted in mice lacking LI1T cells, the possibility thatthese cells act early in an inflammatory response to affect the priming process has not been explored. We will investigate these areas, which are of fundamental importance in understanding host immune defense. eradicate the injurious signal, to promote the expansion of neutrophils and monocytes in the bone marrow and their release and response. IL-17 response at the onset of acute inflammation and we found that DCTr recruitment to sites of inflammation. This process strengthens the inflammatory cascade to response to tissue damage and/or infection. While it is largely an starts the resolution program and in vertebrates, it has evolved to require a T cell cytokine, launches the adaptive immune .2) (U) =w' pay -,Q" ,tea --6 E'6 0 =-0 0-0 ono